In summary, molecular and genetic studies have shown that high-grade ovarian serous carcinomas carry a high prevalence of p53 and BRCA gene mutations but not mutations in KRAS or BRAF oncogenes; on the contrary, low-grade ovarian serous cancer has a frequency of KRAS or BRAF mutations but very rarely mutations in p53 or BRCA1/2 (Table 2), suggesting that high- and low-grade serous carcinomas develop along two distinct pathways. This evidence concerns the gene KRAS and ovarian serous adenocarcinoma.